Methods of use of FGF homologs

Abstract

The present invention relates to methods of using zFGF5 compositions to proliferate chondrocytes and their progenitors, and to induce deposition of cartilage. zFGF5 compositions are disclosed for treating disorders associated with chondrocytes, such as cartilage injuries and defects. In addition, methods for treating neurological disorders, such as stroke, are disclosed, and methods for using zFGF5 compositions to stimulate growth of cells associated with neurological injury and disease are disclosed.

Description

REFERENCE TO RELATED APPLICATIONS[0001]This application is a continuation of U.S. patent application 09 / 634,318 filed Aug. 9, 2000 now abandoned which is a continuation of U.S. patent application Ser. No. 09 / 574,750, filed on May 18, 2000; which is a continuation-in-part of U.S. patent application Ser. No. 09 / 229,947, filed on Jan. 13, 1999, now U.S. Pat. No. 6,518,236; which is a continuation-in-part of U.S. patent application Ser. No. 08 / 951,822, now U.S. Pat. No. 5,989,866, filed on Oct. 16, 1997; and Provisional Application 60 / 028,646, filed on Oct. 16, 1996; for which claims of benefit are made under 35 U.S.C. § 119(e)(1) and 35 U.S.C. § 120, and are incorporated herein by reference in their entirety.BACKGROUND OF THE INVENTION[0002]The fibroblast growth factor (FGF) family consists of at least eighteen distinct members (Basilico et al., Adv. Cancer Res. 59:115–165, 1992 and Fernig et al., Prog. Growth Factor Res. 5(4):353–377, 1994) which generally act as mitogens for a broad ...

AI Technical Summary

Problems solved by technology

However, because infarction and other causes of myocardial necrosis appear to be irreparable, it appears that the normal mechanisms of cardiac hyperplasia cannot compensate for extensive myocyte death, and there remains a need for exogenous factors that promote hyperplasia and ultimately result in renewal of the heart's ability to function.

Stroke is a major health problem disabling over three million people in the United States, with 550,0000 Americans suffering stroke each year, of which 150,000 of those affected will die.

The current treatments to prevent tissue damage resulting from stroke are very limited and require administration within an hour of onset of the stroke.

While there are more drugs available to try to prevent reoccurrence of stroke, they are not without some serious drawbacks, including the development of intracranial hemorrhaging, gastrointestinal bleeding and neutropenia.

When bone resorption exceeds bone formation, a net loss in bone results, and the propensity for fractures is increased.

Replacement of damaged articular cartilage caused either by injury or defect is a major challenge for physicians, and available treatments are considered unpredictable and effective for only a limited time.

While deposition of fibrocartilage is not a functional equivalent of articular cartilage, it is at the present the best available treatment because there has been little success in replacing articular cartilage.

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